In previous studies, we have examined the mechanism of action of aflatoxin at the subcellular level and have found important interactions both with nuclear and with mitochondrial functions. These studies will be primarily focused in the coming year on the role of aflatoxin in modifying the mitochondrial transcription process. The role of metabolism as it is related to carcinogenic potential has also been considered in these studies. Specifically, we have used treatments such as dietary protein deficiency and administration of microsomal enzyme inducers to modify hepatic microsomal enzyme activity, since the effects of these treatments on in vivo aflatoxin hepatocarcinogenesis are known from the work of others. Dietary protein deficiency reduces microsomal enzyme activity in the growing animal partly through an inhibition of liver cell proliferation and partly through an effect on the enzyme system. Further studies are designed to determine how these selected perturbations of microsomal enzyme activity modify aflatoxin metabolism and in turn, what effects such modifications have on selected biochemical systems affected by aflatoxin activity.